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Hi everyone!
I have had MRI's of my brain and spinal cord this spring in preparation for investigating revimmune as a possibility.

I have had a progressive seeming course since spring of '03 (after 12 years of MS before that with a benign course-I have been on Cop since it came out) and at that time I was essentially a 1 or a 2 and I am now on a cane full time.

In '03 I started LDN-- no effect. MR showed slight progression in lesions size. In '05 I started antibiotics which helped with a bunch of symptoms but have not stopped progression (see my regimens log if interested).

My current MRI of my brain is clean, no enhancement no new lesions or expansion of old lesions, no inflammaation, no atrophy nothing. It is unchanged since beginning abx 3 years ago which was the last MRI.

We did a spine MRI set to see if something is going on there to account for the progression, the cervical spine is fine no enhancement no lesions. I have no report yet for the thoracic spine.

THE POINT

In conversation with my doctor yesterday he told me that SPMS is marked by stable appearing MRI's with no new lesions and enhancement but ongoing progression. He told me something I had not heard before: namely that probably MS burns itself out and gets done doing its damage, but the brain continues to deteriorate in the same fashion it does in "post polio syndrome".

For those not familiar with post polio, polio is a virus that attacks people and in a rare person, about 5%, they actually get sicker than the usual "it's a cold" experience and instead get a neurological issue. 2% will have paralysis. The virus goes away and people recover to a greater or lesser degree based on how much damage was done in the active phase.

(isn't it curious that so few get the paralysis when the germ was so common before vaccine? WHy 5% and not all people? Why those specific people? Like MS, twins did not usually both get paralysis so it is not necessarily genetics.........)

People who seemingly recovered very well or even completely in that rare group that actually had some level of paralysis are finding decades later that they are progressively losing ground and function.

This syndrome is not a reactivation of the virus, but is instead deterioration of the 'alternative nerve pathways' the body created in the aftermath of the disease; thus when a nerve was killed by the virus when it was active, a nearby nerve took over the job of the dead nerve, this made that nearby nerve thicker and longer to do the extra work, but eventually the extra effort and oxidative injury from the additional work load takes it's toll and it too dies.

SO my neuro's belief is that the SPMS stage is a similar mechanism in the MS brain.

He essentially said there are no treatment strategies to help this stage of MS. Reducing inflammation will not help because inflammation is not causing any problems now, the problems are something else entirely. IT is degenerative and not inflammatory at this point. So he believes.

I recognize the idea of SPMS being non-inflammatory and have heard of course of the idea that it is a secondary neuro degenerative disease where RRMS is the "real" inflammatory disorder, but I had not heard the idea that the process we call "MS" is over or that it is an entirely different mechanism for the loss of fiunction in other nerves altogether.

This seems a more sinister theory: he is saying essentially that not only have MS nerves been lost, but neuroplasticity has been exhausted and is collapsing too.

Anyway has anyone else heard this post polio like theory and what implications might it have?

If he is right, then SPMS is a completely different disease and the idea that any strategy that help RRMS could help SPMS is completely impossible. Forget about revimmune or any other thing helping SPMS; they will not.

OTOH I suspect he is wrong for these reasons
1. There is degeneration from the beginning, it is not some late stage development; it is part of the disease.
2. Post polio nerve pathways usually work for decades, SPMS is usually much quicker than that.

This suggests to me that the MS process is still there and going on, perhaps the inflammation has "burned out" but not MS. If this is correct then strategies that help RRMS might help SPMS to the degree that it impacts the degenerative component (I am in the "MS is degenerative" camp). Some of our current strategies are neuroprotective; copaxone is neuroprotective (stimulates BDNF), so is minocycline.

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Interesting post. I did alot of reading on polio in the last year. I hadn't heard of any docs likening it to MS, but I posited from my reading that "post polio syndrome" sounded an awful lot like MS... and that MS might just be "post-epstein barr syndrome" or "post cpn infection." It just makes sense to me that some sort of infection begins the process of MS, and leads to the inflammatory stage. After the virus has quieted, the damage continues, just as in post polio syndrome:

Read this, and substitute MS for post polio syndrome....

"PPS is rarely life-threatening. However, untreated respiratory muscle weakness can result in underventilation, and weakness in swallowing muscles can result in aspiration pneumonia.

The severity of residual weakness and disability after acute poliomyelitis tends to predict the development of PPS. Patients who had minimal symptoms from the original illness will most likely experience only mild PPS symptoms. People originally hit hard by the poliovirus and who attained a greater recovery may develop a more severe case of PPS with a greater loss of muscle function and more severe fatigue. It should be noted that many polio survivors were too young to remember the severity of their original illness and that accurate memory fades over time.

According to estimates by the National Center for Health Statistics, more than 440,000 polio survivors in the United States may be at risk for PPS. Researchers are unable to establish a firm prevalence rate, but they estimate that the condition affects 25 percent to 50 percent of these survivors, or possibly as many as 60 percent, depending on how the disorder is defined and which study is quoted."

People "hit hard" with the original virus and who recovered (many lesions at presentation with no more inflammation) will continue to degenerate (into a primary progressive form) I think your neuro is, sadly, onto something.

Where I respectfully disagree with your neuro is in the idea that plasticity is eventually exhausted. I remain convinced that the brain is able to continually reroute (the spine is more difficult), however we are just beginning to understand the process.

I also hope that an anti-viral protocol can slow the degenerative process, and anti-oxidants can aid the damage repair. Actually, I'm banking on it for my husband...

I'm sorry for your current difficulties, Marie. I still believe hicy will prove to be of benefit for progressive MSers. It may not be a cure, but it should alleviate further deterioration. And plasticity will make up for some of the damage. I hope/pray for all of us that JH will treat progressive folks. My husband's MRI has gone quiet, but I'm afraid his disease continues. I keep my eyes on the horizon.
AC

Marie, I hadn't heard of the post polio syndrome, but he mother of one of my friends had polio in late adolescence and came out of it with what seemed like complete recovery, the only deficit being one leg slightly shorter than the other, giving her slight limp. This became more noticeable over time, but I can't say it was due to anything more than being very overweight and not liking to use a cane. She wasn't really affected mentally at all until she had two very bad strokes, but again these could have happened anyway.

Now, going on to MS, when I was eventually diagnosed with secondary progressive disease, I had many large lesions in the brain. Many of these were very bright and therefore active and therefore one would assume, an inflammatory process was active. Six months later, after starting on doxycycline and roxithromycin and having done about four metronidazole pulses, these were far less bright and there were no new ones. The radiologist was so amazed by this that he did a series of scans on check on progress. Over a period of two years there were no new lesions and some of the newer ones disappeared altogether. Now, five years after starting this treatment, one year of these without taking anything, my disease has not got worse at all. I have regained the use of my nearly paralysed right arm and am not impaired at all cognitively. My walking is still not perfect, but is far better than it was. My hyper-reflexia has all but gone. Apart from the antibiotics I have been taking supplements known to work on inflammation and these I have continued to a lesser extent since finishing treatment. Therefore I do feel that it is wrong to say that SPMS doesn't have at least some inflammatory component. I don't think your neurologist can be right: mine developed gradually into the progressive phase over a number of years. When was the point when it became this different disease? I don't suppose my walking will ever be absolutely perfevct but I am right in so many other respects, it ceases to be greatly important. The biggest thing, as a professional fine-artist is that I can paint again and better than ever.

Sarah

An Itinerary in Light and Shadow Completed Dr Charles Stratton / Dr David Wheldon abx regime for aggressive secondary progressive MS in June 2007, after four years. Still improving with no relapses since starting. Can't run but can paint all day.

Post polio syndrome is very real, but it affects only 25-50% of polio survivors. It seems to affect those who had the greatest recovery after the initial presentation of the polio virus. The non-inflammatory progression of MS probably affects the same percentage of MSers. Not everyone.

I don't think Marie's neuro is saying that all SPMS is the same, Sarah. He is referring to the type of disease where inflammation ceases, yet disability progresses. This is a very different course than your MS. At the risk of sounding Finn-like...
http://www.springerlink.com/content/u14247427041756l/

You are incredibly fortunate, Sarah. But everyone' s MS course is different. A cpn infection will respond to antibiotics, as you have proven. A viral course (or post-EBV as I posit) of MS will not.
respectfully,
AC

Sarah thanks for adding your experiencess here. I did point out that I have had no inflammation no new lesions at all in the 3 years since I have been on abx. Of course you know I have done antibiotics for 3 years. I am still on them, they have helped me greatly (clarity, energy, spasms).

But the question has to do with progression. I am still progressing; no sense denying it, so perhaps there is more going on in my brain than what an antibiotic can impact on its own. Is it a virus that is part of the overall issue in my case as different from yours? Luccinetti says there are 4 types of lesions, does that mean 4 distinct causes?

Is it that the neuro is right and in some people's case a PPS type activity is the mechanism of ongoing losses? If so, maybe the antibiotics have worked great for me and the fact of progression is a separate issue altogether. In that case a person could not "tell" if abx worked for them based on symptoms.

In that case too a person might get better with abx but the progression at least would be limited to what you had lost before...assuming that CPn is the germ and it was defeated but you progress based on the PPS idea. SUch losses would be limited.

We need more pathology! Balin has picture of CPn in AD lesions, we need that here! That or something else clarifyig things

Cheer, Thanks for the response, a debate is what I hoped we'd have on this subject.
I still offer this: if MS is an inflammatory disease and that is the main mechanism (I think it is not, I think it is degenerative disease due to some kind of infection and inflammation secondary to that, but we seem to be in the same camp there) then the worst you would have to worry about in SPMS is the return of your worst symptom.

You could not get a new symptom because what would happen is the workaround nerves fail so you fall back to your worst day but no further.

But people with SPMS do get new symptoms and new areas of involvement so the initial activity must go on in spite of lack of inflammation. Therefore what ever MS is, germ, metabolic problem, post viral autoimmunity, it is still going on without the body responding to it with inflammation in SPMS.

Interesting abstract you linked saying that 50% of people get SPMS pre the days of CRABS. It will be interesting to see if that number changes....either way.

I am feeling snarky so I will add my cynical concern that the antiinflammatory approaches may mean more conversion to SPMS. My benign MS is certainly not now, and I've had 11 years of copaxone as well as methotrexate and prednisone for exacerbations. Antibiotcs likewise are considered antiinflammatory as well.

I was told when I went on cop because we caught it so very early I would likely not ever get bad....maybe a cane at 60. Well, that was sure wrong!

I am sorry to hear of your current status. It also echos my worst fears. I am faring quite well right now, but hearing of cicumstances such as yours really alarm me. I just wonder if that is what the future holds for me as well. I am on Minocyclyine ABX right now. I am currently at an EDSS of 0. I really have no deficits right now. It has been 3 years since I was diagnosed. I just wonder if I will suddenly start to deteriorate?

It is facinating to see how MS works, but also scary. It is such a cruel disease.

I would question 1) why does SPMS respond to some treatments? Your neuro's theory sets up an absolute that does not exist. There are very few and only partially effective treatment for SPMS is not even remotely the same as nothing we can do can touch it. and 2) Nerves pick up the slack from the damaged areas but eventually collapse under the strain... ok so when those go under why aren't there more to pick it up again?

I do think the PPS comparison is a good one. Just some of those particulars strike me as absolutes.

Hi Marie, yes I am aware of all the benefits you have gained through being on antibiotics and I know you are still on them, but I just wanted to make you say so on the general forum.

I also know that they haven't totally stopped your progression: your mind might not be getting worse but your mobility is, so obviously something else is going on, but what? Its very easy for neurologists to say that when you have got fully into the progressive stage of the disease, there is nothing that really can be done: mine, ex Queen's Square but now at Addenbrokes, birthplace of Campath, was a past master a that kind of talk.

I do still feel that something like Revimmune holds benefit for people like you, once you have off-loaded the ineffective cause. If you went into it too soon, though, the infection will still be there in the background and will eventually regroup. This is in several people's minds as to what happened in the early days of Campath, when it was tried on a group of SPMS people. All well and good at first and the same benefits were seen in some as primary progressive people are now finding, but they ended up getting worse:

However, more mixed results were seen in a study of 25 people with secondary progressive MS. MRI scans over seven years showed no new lesions forming in the brains and spinal cords of those participants who had been treated with alemtuzumab, but the people on this trial continued to accrue disability. This led researchers to the idea that something other than inflammation of myelin is at work in progressive MS. Consequently, they have looked at whether alemtuzumab works best if used early in relapsing/remitting forms of MS.

I guess this is why the Revimmmune people re not rushing to try it on people with progressive disease, or at least I hope that is their reason.

Now, we both started off with benign MS, you took copaxone and all, I took nothing but we both ended up very much worse for whatever reason. We then both started abx and both have benefited greatly, except mobility wise you are still progressing and I am not, although I haven't improved as much as I. the perennial optimist, might have liked. I never had any rheumatoid arthritis like you or in fact any pains at all and I never got any childhood diseases except scarlet fever, so maybe it is to do with not having a bunch of coinfections, or having been able to hold things like varicella zoster and EBV, both of which most people come across in childhood or adolescence, at bay.

We do need more biopsies or autopsies to help provide some evidence, but autopsies are somewhat falling out of favour.

Sarah

An Itinerary in Light and Shadow Completed Dr Charles Stratton / Dr David Wheldon abx regime for aggressive secondary progressive MS in June 2007, after four years. Still improving with no relapses since starting. Can't run but can paint all day.

I wanted this thread to be about PPS vs SPMS rather than abx but Cheer asked if I still am of the same mind I was in a thread two years ago in which the idea that MS might be caused by CPn was discussed.

I still believe the theory that MS is possibly caused by a cryptic bacteria is perfectly plausible. It is clear that many people have had good success using that approach, others, like me, continued to progress in terms of motor function.

The problem is that it is possible antibiotics were working fine for me in this context: If MS is caused by a cryptic bacteria, then when the inactive non metabolizing bacteria is finally killed by abx, the cell that it lived in will die. This could result in deteriorating function; it depends on which cell was impacted.

Of course, the biggest problem with using antibiotics for MS is that we do not have a proven hypothesis, we do not have indusputable pictures of CPn in the microglia adjacent to MS lesions (this is difficult to get so not surprising) and while researchers in many places have found evidence of CPn in MS brains, not all people looking for it have found it. So it remains a possibility but not a proven theory.

If you decide to use a therapy like the VU abx protocol for MS, you can do it under only one possible gauge for success: empirical treatment; in other words, does it help me.

In my case, I have no expanded lesions, no new lesions, no atrophy and completely stable MRI findings with no enhancement comparing a new MRI with the one at start of abx 3 years ago. I have a black hole in the middle of the largest lesion which I had when I began antibiotics. It is probably that area that is responsible for the motor problems.

I also have enjoyed much better physical comfort in that abx result in reduced spasms for me, which in my world is a big deal. I also have more energy and less "brain fog", which is that sense that you are kind of outside looking in and far away from life and getting further every day--a slippng away feeling. That's gone too. I really feel a lot better on abx overall.

But the progression poses a dilemma for me. It can't prove or disprove the CPn/cryptic bacteria hypothesis for MS, but if you continue to have motor losses, what do you do? What do I do?

My neuro, who BTW said the abx are simply antiinflammatory (he is not the prescribing physician for that), said I have stable MS but the losses I have experienced are simply this PPS type event which is why I started this thread. I wanted to know if others had heard this.

Of course, if he is right that SPMS is the same mechanism as PPS, then it is enitrely possible that abx worked fine and stopped MS in its tracks, but the SPMS phase will continue unabated because it is a totally different mechanism for motor losses. If he is correct SPMS will be a tough nut to crack.

Just for grins, I will mention that the neuro said to me:

"well tysabri is the only thing we might consider but you really have no inflammation and it is not typically effective in that situation."

I suggested revimmune because it kills peripheral immune cells (and CPn lives in peripheral immune cells and EBV lives in b-cells so two vecters for infection could potentially be eliminated with that approach) and because the people posting on that forum are saying it is very effective.

he said "That is a bad idea, I'd be concerned about bladder cancer 10 years down the road or other cancer or problems. If you get any worse we will do tysabri"

I said I thought you said it will not help considering the lack of inflammation...

he said "well we can try it and see, it might help....if you get any worse or seem to be slipping." (I'm about an EDSS 6 BTW-not a lot of 'worse' to go)

It MIGHT help. OK so that is advice from a neurologist who is recently here on his own as a local MD from an MS clinic in the nearby large city. He is no dummy and is very up on all the research and clearly can rattle off rapid fire the most recent findings with stunning accuracy and recall.

But do you see the conundrum? Why is my "unproven approach" stupid and his (application of an approved drug for a known ineffective application) a smart and acceptible move?

In Sarah's post above, she linked a quote from a research paper on campath showing that SPMS patients got worse on that drug in spite of no lesion formation. Since tysabri like campath has considerable side effects, is the risk vs reward ratio in my favor if I do his approach?
Since abx really have no serious side effects, how about the risk/reward for that idea? I already know they help me in some areas....

I wish we had more data to go on with regards to the idea that cryptic bacteria are at the heart of MS. If we had more generally accepted data supporting the idea of cryptic bacteria, we would just accept that the motor losses are part of the process and go on.

In my personal situation I need to decide what strategy to try to apply at this point and the mixed results I have had with abx- both some things better and some motor losses -make it hard to know what to do. As it is, I am still on abx (and copaxone BTW-for 11 years).

There are no approved therapies for SPMS unless you try novantrone and I do not want to do that because its results are again related to inflammation and it has cardiotoxicity-my family history suggests this is not probably a good route for me and my neuro actually has had all 4 patients he ever prescribed it to get that complication and 3 of them had no results from the drug as far as MS goes.

That's not what the marketing department of the drug tell you and it is not what we want to hear but it was his experience and he will not prescribe it.

At any rate I hope that answers Cheer's question. Honestly if I had not done abx and there was another person on this board like me who had posted about it, I'd want to know what happened at the 3 year point too, so maybe this diversion was worthwhile to discuss.

Brock, if I could go back in time to my "3 years post diagnosis self" this is what I would say: You will be fine for a long time (I could still jog and did 3 times a week right up to 6 years post diagnosis--I still jogged but sporadically after that, because we moved, for probably another 3 years) Take the best care of yourself that you can in terms of nutrition and health otherwise and also LIVE! Do fun stuff and enjoy every second of your life. Get exercise as possible (this is good for neurotropic factors) and be as strong and flexible as you can physically. Nurture every person in your life and hold them dear, including yourself. Focus on the things you are grateful for and stop obsessing about what might happen because it might not.

I would also loosen up a little moola for a cruise when I was still more mobile. It sounds not too fun now, but I wanted to see the glaciers in Alaska once.

Please believe you will be flexible enough and resourceful enough to cope with whatever you have to as it comes along. ANd be kindof lucky feeling in that there is a lot of good stuff coming along even as you read this. I got sick in '91. That was a LOOOOONG time ago! If you are as I was, 15 years from now you'll still be a walking functioning person, even if you use a cane as I do. But I assume we'll get more information long before then. If nothing else stem cells are coming pretty soon as well as other regenerative strategies for nerves...

At any rate that is the long drawn out expanation of Cheer's question.

I hope anyone else who has thoughts about the PPS vs SPMS question posts their understanding.......
marie

Hi Marie-
I honestly didn't mean to change the thread direction to abx, not the intent of my question...I only wanted to hear what you've learned.
Thanks for long and drawn out response. I truly appreciate your honest answers. I'm sure many others will, as well. I am so sorry for your progression. I can only imagine how difficult and discouraging it must be to lose your mobility. I hope I didn't seem too provocative, but my husband was only diagnosed last year, and I really want to learn as much as I can.

The neuro told my husband at diagnosis..."Do all you can NOW. Don't put anything off." He presented with so many lesions and so much damage, she was amazed at his lack of disability. We took his family to Austria that summer, and he has traveled the world over in the year since. He keeps working, and biking, and enjoying everyday. I don't have a crystal ball, and maybe that's a good thing, but he is taking supplements, eating the Swank diet, writing beautiful music, taking his daily copax shots, and feeding his mind and soul. We remain hopeful.

I do believe that there is a bacterial component for many with MS, be it lyme bacterium, cpn, or other chronic spirochetal infections. I also believe my husband's MS process began with a viral disease, since he had mono as a young adult, and was almost killed by a virus as an infant. I think MS is a fingerprint disease, and with a bit of sleuthing and process of elimination, one can ferret out how their disease activated. But I may be completely off base-

The reason this post polio supposition struck me, is because it was only in the last century Jonas Salk isolated the polio virus and created a vaccine. Because I am a mom, I look at my child, and imagine a world free of cancer and B-cell disease, for his children, for all our children. I wonder why polio developed in only 5% of those exposed to the virus...why some teens get mono and are over it, why some develop MS. Why does cpn give some people pneumonia, and others MS?

The medical community is as stymied by these questions as we all are. It's my sincere hope this dialogue will help all of us.

Growing up in a mixed Catholic/Jewish home...I have no problem seeing many sides of an issue. Debate was an art form in our house! I do not believe that positing MS begins as a virus in some, precludes a bacterial component in others. There are many ways to see this problem...but I fear that folks get into their "fundamentalist" ways of thinking, and write off the other guy as a quack or wacko. We've seen it happen on many of these threads. And it happens in the medical community, as your neuro's reaction to Revimmune proves.

Rainer,
good points. I agree with you it seemed unrealistically absolute. I do not agree that SPMS is the same anyway as I think more about it and come to terms with the actual dx of SPMS and a new neuro whose approach seems to be "I hope you've accepted your fate............" I ditched neuro number one in '94 for better neuro #2 whose attitude was positive. I may need to do that again . Thanks for helping me think about things.!

Cheer,
I am pleased to be able to offer some thought from my personal experience. If nothing else with this darned disease at least we can share what our personal experiences are, and that sharing leaves us less isolated.

CHEER said

Hi Marie- I honestly didn't mean to change the thread direction to abx, not the intent of my question...I only wanted to hear what you've learned.

It is OK I am happy to share, but the abx ideas can get some folks really hot under the collar. I am really averse to confict and run the other way .

To the PPS thing, I have been thinking and thinking on it and there are a couple of things that counter it, one is that we know degeneration is present from the earliest stages of MS, it is not a late development. So since that is true then MS is not a purely inflammatory disease but a combination inflammatory and degenerative disease (lots of research papers say so, and especially recently).

It is the degenerative componenet that we have so little understanding of. It is an utter mystery in terms of real evidence. In my mind it is the key to the whole thing, figure that out and you have the disease whipped.

And to assume that late degeneration, like that at the SPMS stage, is somehow different and a new type of degeneration as my neuro did seems presumptuous considering the lack of pathology evidence for it, heck they don't even have pathology for the initial degenerative component of MS. It seems more plausible that the degenerative component of MS that was there all along is the likely component of the SPMS degeneration. Why not? why would it change to another type of degeneration?

and also I know people with PPS. They have this issue very late in life, MSers have this happen early in life. Why would a nerve "workaround" fail in 10 years in an MSer when it lasts 40-50 years in a PPS person?

You might say well the MS process is going on, but WAIT, the "MSprocess" is supposed to be inflammation and we've already determined and stated that SPMS is marked by lack of inflammation.
If MS is a combination inflammatory/degenerative disease and the inflammatory process ends, what are you left with? degeneration.

Buying the neurologist's theory that MS burns itself out and SPMS is like PPS, if there is not inflammation and the "MS process" has burned itself out and now you are just stuck with SPMS which is a degeneration of the workaround nerves, then they should last as long as polio survivers nerves do and they should only break down to the extent that the original exacerbations did.

In other words once you reach the SPMS phase in that model it should mean things calm down a lot and you should stay at that functional level for decades, only to maybe lose ground in old age to the level of your worst exacerbation because that is the only area of these workaround nerves .

MS would not be the feared disease it is if that was true and people would look forward to the SPMS phase because it would mean the end to new losses, although you potentially could lose as much as you had in your worst exacerbation.

I kind of think he is wrong about the PPS idea. I bet there is some loss along those lines, but my guess is that it is in addition to the regular degeneration of MS, that it occurs in late years and it is probably invisible by that time in the MSers life.

The positive thing in that is that some of the drugs for RRMS might help SPMS too if they are regenerative and protective as well as antiinflammatory.
THoughts? flaws in my logic?
marie

Thank you for your advice. I know that is the right way to live, regardless of this stupid disease. On a daily basis I don't really even think about it that much, but I do think about it. I visit this site almost every day, and every day I wake up and still have all of the functions I had the day before, I am grateful, and give out a sigh of relief, literally.

I will not give you my pity, but instead my respect. You have a really good attitude about everything, and seem to be a very strong person. I agree with you that even if I do progress, if/when that may be, I'll still keep going until I can't go anymore. Hopefully all of us will see some answers in the near future that will actually help us.

I still think that MS is more related to some infectious cause as opposed to autoimmune. Infact I think a lot of the conditions they say are autoimmune are actually of infectious pathology.

More than anything, as I have said before, this site is my home. It helps to read everyones perspectives, and to also learn about this disease. I can also say that thisisms.com has to be about the most up to date source for MS that is out there. I don't contribute very much, but i am extremely grateful for the support I have received from all of the members here.

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